Amino Acid Chloromethyl Ketones
Cysteine Proteinase Inhibitors
Proto-Oncogene Proteins c-bcl-2
Cytochrome c Group
X-Linked Inhibitor of Apoptosis Protein
Apoptotic Protease-Activating Factor 1
bcl-2-Associated X Protein
Inhibitor of Apoptosis Proteins
In Situ Nick-End Labeling
BH3 Interacting Domain Death Agonist Protein
Apoptosis Regulatory Proteins
Fas-Associated Death Domain Protein
Apoptosis Inducing Factor
Tumor Cells, Cultured
CASP8 and FADD-Like Apoptosis Regulating Protein
Membrane Potential, Mitochondrial
TNF-Related Apoptosis-Inducing Ligand
Reactive Oxygen Species
Tumor Necrosis Factor-alpha
CRADD Signaling Adaptor Protein
Intracellular Signaling Peptides and Proteins
Death Domain Receptor Signaling Adaptor Proteins
Dose-Response Relationship, Drug
CARD Signaling Adaptor Proteins
bcl-2 Homologous Antagonist-Killer Protein
Tumor Suppressor Protein p53
Receptor-Interacting Protein Serine-Threonine Kinases
Antineoplastic Agents, Phytogenic
RNA, Small Interfering
Amino Acid Sequence
Receptors, Tumor Necrosis Factor
Receptors, TNF-Related Apoptosis-Inducing Ligand
bcl-Associated Death Protein
Molecular Sequence Data
JNK Mitogen-Activated Protein Kinases
Adaptor Proteins, Signal Transducing
Protein Structure, Tertiary
Reverse Transcriptase Polymerase Chain Reaction
Receptor-Interacting Protein Serine-Threonine Kinase 2
Protein Synthesis Inhibitors
Myeloid Cell Leukemia Sequence 1 Protein
Protein Processing, Post-Translational
Mitogen-Activated Protein Kinases
Receptors, Death Domain
Proto-Oncogene Proteins c-akt
Drug Screening Assays, Antitumor
Receptors, Tumor Necrosis Factor, Type I
p38 Mitogen-Activated Protein Kinases
Disease Models, Animal
Proteasome Endopeptidase Complex
Drug Resistance, Neoplasm
Gene Expression Regulation
Endoplasmic Reticulum Stress
Recombinant Fusion Proteins
Cell Line, Transformed
Sequence Homology, Amino Acid
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Protein Kinase C-delta
Gene Expression Regulation, Enzymologic
Lamin Type B
MAP Kinase Signaling System
Xenograft Model Antitumor Assays
Mitogen-Activated Protein Kinase 8
MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (1/2233)Amplification of the MYCN gene is found in a large proportion of neuroblastoma and considered as an adverse prognostic factor. To investigate the effect of ectopic MycN expression on the susceptibility of neuroblastoma cells to cytotoxic drugs we used a human neuroblastoma cell line harboring tetracycline-controlled expression of MycN. Neither conditional expression of MycN alone nor low drug concentrations triggered apoptosis. However, when acting in concert, MycN and cytotoxic drugs efficiently induced cell death. Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. Loss of mitochondrial transmembrane potential and release of cytochrome c from mitochondria preceded activation of caspase-8 and caspase-3 and cleavage of PARP. CD95 expression was upregulated by treatment with cytotoxic drugs, while MycN cooperated with cytotoxic drugs to increase sensitivity to CD95-induced apoptosis and enhancing CD95-L expression. MycN overexpression and cytotoxic drugs also synergized to induce p53 and Bax protein expression, while Bcl-2 and Bcl-X(L) protein levels remained unchanged. Since amplification of MYCN is usually associated with a poor prognosis, these findings suggest that dysfunctions in apoptosis pathways may be a mechanism by which MycN-induced apoptosis of neuroblastoma cells is inhibited. (+info)
Identification of an endogenous dominant-negative short isoform of caspase-9 that can regulate apoptosis. (2/2233)Alternatively spliced isoforms of certain apoptosis regulators, such as Bcl-x, Ced-4, and Ich-1, have been shown to play opposing roles in regulating apoptosis. Here, we describe the identification of an endogenous alternatively spliced isoform of caspase-9, named caspase-9b, which lacks the central large subunit caspase domain. Caspase-9b is detectable in many cell lines by PCR and at the mRNA and protein levels. Caspase-9b can interact with the caspase recruitment domain of Apaf-1, and like the active site mutant of caspase-9, it can inhibit multiple forms of apoptosis, including those triggered by oligomerization of death receptors. It can also block activation of caspase-9 and -3 by Apaf-1 in an in vitro cytochrome c-dependent caspase activation assay. These results suggest that caspase-9b functions as an endogenous apoptosis inhibitory molecule by interfering with the formation of a functional Apaf-1-caspase-9 complex. (+info)
Caspase-9 can be activated without proteolytic processing. (3/2233)The recombinant form of the proapoptotic caspase-9 purified following expression in Escherichia coli is processed at Asp315, but largely inactive; however, when added to cytosolic extracts of human 293 cells it is activated 2000-fold in the presence of cytochrome c and dATP. Thus, the characteristic activities of caspase-9 are context-dependent, and its activation may not recapitulate conventional caspase activation mechanisms. To explore this hypothesis we produced recombinant forms of procaspase-9 containing mutations that disabled one or both of the interdomain processing sites of the zymogen. These mutants were able to activate downstream caspases, but only in the presence of cytosolic factors. The mutant with both processing sites abolished had 10% of the activity of wild-type, and was able to support apoptosis, with equal vigor to wild-type, when transiently expressed in 293 cells. Thus caspase-9 has an unusually active zymogen that does not require proteolytic processing, but instead is dependent on cytosolic factors for expression of its activity. (+info)
Tumor necrosis factor alpha regulation of the FAS-mediated apoptosis-signaling pathway in synovial cells. (4/2233)OBJECTIVE: Fas-mediated apoptosis is observed in synoviocytes of patients with rheumatoid arthritis (RA), but not in those of patients with osteoarthritis (OA). The present study was conducted to elucidate the mechanisms that initiate induction of Fas-mediated apoptosis in RA synoviocytes. METHODS: Cultured OA synoviocytes, which are insensitive to Fas-mediated apoptosis in spite of Fas antigen expression, were used in these experiments. Synovial cell proliferation and cytotoxicity studies were performed using MTS and lactate dehydrogenase release assays. Surface expression of Fas antigen was analyzed by flow cytometry. The expression and function of apoptosis-signaling molecules, such as caspase 8 and caspase 3, were examined by immunoblot analysis. RESULTS: Tumor necrosis factor alpha (TNFalpha) induced proliferation of cultured OA synoviocytes. Fas ligation with anti-Fas monoclonal antibody (mAb) resulted in cytotoxic activity against cultured OA synoviocytes that had been pretreated with TNFalpha for 5 days, but not those pretreated for 2 days. In contrast, anti-Fas mAb did not show a cytotoxic effect against untreated cultured OA synoviocytes. A gradual up-regulation of caspase 8 and caspase 3, which played a role in the caspase cascade for Fas-mediated apoptosis, was observed in TNFalpha-treated cultured OA synoviocytes. In addition, Fas ligation to TNFalpha-treated cultured OA synoviocytes induced activation of caspase 8 and caspase 3, with subsequent cleavage of poly(ADP-ribose) polymerase (PARP), a substrate of activated caspase 3. More importantly, Z-IETD-FMK, a caspase 8 inhibitor, and Ac-DEVD-CHO, a caspase 3 inhibitor, almost completely inhibited Fas-mediated apoptosis of TNFalpha-treated cultured OA synoviocytes, whereas Ac-YVAD-CHO, a caspase 1 inhibitor, did not. CONCLUSION: Our results clearly demonstrate that TNFalpha stimulates synovial cells to proliferate as well as sensitizes the cells for Fas-mediated apoptosis, at least in part by up-regulation and activation of caspase 8 and caspase 3. These findings suggest that TNFalpha may be one of the factors providing sensitization of synovial cells to Fas-mediated apoptosis in RA. (+info)
Solution structure of BID, an intracellular amplifier of apoptotic signaling. (5/2233)We report the solution structure of BID, an intracellular cross-talk agent that can amplify FAS/TNF apoptotic signal through the mitochondria death pathway after Caspase 8 cleavage. BID contains eight alpha helices where two central hydrophobic helices are surrounded by six amphipathic ones. The fold resembles poreforming bacterial toxins and shows similarity to BCL-XL although sequence homology to BCL-XL is limited to the 16-residue BH3 domain. Furthermore, we modeled a complex of BCL-XL and BID by aligning the BID and BAK BH3 motifs in the known BCL-XL-BAK BH3 complex. Additionally, we show that the overall structure of BID is preserved after cleavage by Caspase 8. We propose that BID has both BH3 domain-dependent and -independent modes of action in inducing mitochondrial damage. (+info)
Solution structure of the proapoptotic molecule BID: a structural basis for apoptotic agonists and antagonists. (6/2233)Members of the BCL2 family of proteins are key regulators of programmed cell death, acting either as apoptotic agonists or antagonists. Here we describe the solution structure of BID, presenting the structure of a proapoptotic BCL2 family member. An analysis of sequence/structure of BCL2 family members allows us to define a structural superfamily, which has implications for general mechanisms for regulating proapoptotic activity. It appears two criteria must be met for proapoptotic function within the BCL2 family: targeting of molecules to intracellular membranes, and exposure of the BH3 death domain. BID's activity is regulated by a Caspase 8-mediated cleavage event, exposing the BH3 domain and significantly changing the surface charge and hydrophobicity, resulting in a change of cellular localization. (+info)
Nitric-oxide-induced apoptosis in human leukemic lines requires mitochondrial lipid degradation and cytochrome C release. (7/2233)We have previously shown that nitric oxide (NO) stimulates apoptosis in different human neoplastic lymphoid cell lines through activation of caspases not only via CD95/CD95L interaction, but also independently of such death receptors. Here we investigated mitochondria-dependent mechanisms of NO-induced apoptosis in Jurkat leukemic cells. NO donor glycerol trinitrate (at the concentration, which induces apoptotic cell death) caused (1) a significant decrease in the concentration of cardiolipin, a major mitochondrial lipid; (2) a downregulation in respiratory chain complex activities; (3) a release of the mitochondrial protein cytochrome c into the cytosol; and (4) an activation of caspase-9 and caspase-3. These changes were accompanied by an increase in the number of cells with low mitochondrial transmembrane potential and with a high level of reactive oxygen species production. Higher resistance of the CD95-resistant Jurkat subclone (APO-R) cells to NO-mediated apoptosis correlated with the absence of cytochrome c release and with less alterations in other mitochondrial parameters. An inhibitor of lipid peroxidation, trolox, significantly suppressed NO-mediated apoptosis in APO-S Jurkat cells, whereas bongkrekic acid (BA), which blocks mitochondrial permeability transition, provided only a moderate antiapoptotic effect. Transfection of Jurkat cells with bcl-2 led to a complete block of apoptosis due to the prevention of changes in mitochondrial functions. We suggest that the mitochondrial damage (in particular, cardiolipin degradation and cytochrome c release) induced by NO in human leukemia cells plays a crucial role in the subsequent activation of caspase and apoptosis. (+info)
Targeted disruption of caspase genes in mice: what they tell us about the functions of individual caspases in apoptosis. (8/2233)Cysteine proteases of the caspase family are crucial mediators of apoptosis. All mammalian cells contain a large number of caspases. Although many caspases are activated in a cell committed to apoptosis, recent data from caspase gene knockout mice suggest that individual caspases may be involved in the cell and stimulus-specific pathways of cell death. The gene disruption studies also establish the functional hierarchy between two structurally distinct classes of caspases. The present review discusses these recent findings and elaborates on how these mutant mouse models have helped the understanding of the mechanisms that govern programmed cell death in the immune and other systems. (+info)
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Loss of appetite
* Weight loss
* Bone pain
* Swelling in the abdomen or neck
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
Death regulator Nedd2-like caspase
Clostridium difficile toxin A
Bcl-2-like protein 1
Proto-oncogene tyrosine-protein kinase Src
Fragmentation (cell biology)
Pattern recognition receptor
Induction of Inflammation by West Nile virus Capsid through the Caspase-9 Apoptotic Pathway - Volume 8, Number 12-December 2002...
Developing a circularly permuted variant of Renilla luciferase as a bioluminescent sensor for measuring Caspase-9 activity in...
Adrenergic stress constrains the development of anti-tumor immunity and abscopal responses following local radiation | Nature...
Deficiency in caspase-9 or caspase-3 induces compensatory caspase activation - CSHL Scientific Digital Repository
Nod1, an Apaf-1-like activator of caspase-9 and nuclear factor-κB - Tohoku University
Corrigendum to "Caspase 9 is constitutively activated in mouse oocytes and plays a key role in oocyte elimination during...
AbMiner - Antibody Detail | Genomics and Pharmacology Facility
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MedlinePlus: Genes: C
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Anticancer effect of involucrasin A on colorectal cancer cells by modulating the Akt/MDM2/p53 pathway
New Eye Drops May Prevent a Common Cause of Blindness | National Eye Institute
PA-10-035: Prioritizing Molecular Targets for Cancer Prevention with Nutritional Combinations (R01)
glial cell apoptotic process Antibodies | Invitrogen ...
XIAP gene: MedlinePlus Genetics
Michael Vogelbaum | Moffitt
Apoptosis-induced nuclear expulsion in tumor cells drives S100a4-mediated metastatic outgrowth through the RAGE pathway - PubMed
Nanoparticles of Titanium and Zinc Oxides as Novel Agents in Tumor Treatment: a Review | SpringerLink
NIOSHTIC-2 Search Results - Full View
minocycline - Ontology Report - Rat Genome Database
Xenopus Anatomy Ontology: Papers for retinal rod cell
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Genentech: Domagoj Vucic | Senior Fellow, Immunology Discovery
- Integration of GWAS and human kidney expression of quantitative trait analysis using Bayesian colocations, transcriptome-wide association studies, and summary-based Mendelian randomization studies prioritized caspase-9 (CASP9) as a kidney disease risk gene. (nih.gov)
- Studies to date have shown the role of caspase-8 (CASP8) and caspase-9 (CASP9) in carcinogenesis. (nih.gov)
- Influence of survivin (BIRC5) and caspase-9 (CASP9) functional polymorphisms in renal cell carcinoma development: a study in a southern European population. (cdc.gov)
- ghaffari moghadam M, abedi B, banaeifar A. The effect of high intensity interval training on the expression of Caspase 3 and 9 horseshoe protein genes in male rats. (ac.ir)
- One-way analysis of variance to compare the expression of caspase 3 and 9 horseshoe protein in male rats in the three groups of high-intensity intermittent exercise, control and control of diabetic basal showed a significant difference between the three means of the group (p = 0.001). (ac.ir)
- Rho-associated protein kinase 1 (ROCK-1) is a major downstream effector of the small GTPase RhoA and a direct substrate of caspase-3. (nih.gov)
- MeHg also induced an increase in mitochondrial-dependent caspase-9 and caspase-3, while the levels of RhoA protein expression were reduced or unchanged. (nih.gov)
- 1. Matrin 3 is a Ca2+/calmodulin-binding protein cleaved by caspases. (nih.gov)
- 12. Specific proteolysis of the A-kinase-anchoring protein 149 at the Asp582 residue by caspases during apoptosis. (nih.gov)
- Our data suggests that on initial exposure to influenza virus, host cells upregulate COX6C mRNA expression through silencing miR-4276 and repressed viral replication by inducing the apoptotic protein caspase-9. (cdc.gov)
- Bcl-x is a pro-survival protein that opposes the pro-apoptotic action of Bax which interacts with mitochondria to activate the caspase 9 pathway. (nih.gov)
Enzymes called caspases2
- The team focused on another group of enzymes called caspases that are known to be important for inflammation and thus might also serve as useful therapeutic targets. (nih.gov)
- It helps protect these cells from self-destructing (undergoing apoptosis) by blocking (inhibiting) the action of certain enzymes called caspases, which are necessary for apoptosis. (nih.gov)
- 28. Reduction of miR-21 induces glioma cell apoptosis via activating caspase 9 and 3. (nih.gov)
- L-asparaginase from human breast milk Lactobacillus reuteri induces apoptosis using therapeutic targets Caspase-8 and Caspase-9 in breast cancer cell line. (bvsalud.org)
- We have previously shown that silica particles, a ubiquitous occupational fibrogenic agent that induces inflammatory responses through microtubule alterations, may activate caspase cascade leading to cell apoptosis. (cdc.gov)
- Taken together, the p38-MAPK pathway is required in oridonin-induced pancreatic cancer cell apoptosis, and which is dependent on its downstream target p53 and caspase activation. (spandidos-publications.com)
- deficiency in caspases essential for this pathway, caspase-9 or caspase-3, unexpectedly resulted in rapid activation of alternate caspases after injection of Jo2, and therefore failed to protect mice against Jo2 toxicity. (cshl.edu)
- Moreover, both ultraviolet and gamma irradiation, two established inducers of the mitochondrial caspase-activation pathway, also elicited compensatory activation of caspases in cultured caspase-3(-/-) hepatocytes, indicating that the compensatory caspase activation was mediated through the mitochondria. (cshl.edu)
- an expression level of pro-caspase-9 cleavage products (35-37 kD) was compared to 3′-terminal deletion mutant, pcWNV-Cp∆3′ (Cp∆3′) and pcDNA3.1 by Western blot analysis with anti-human caspase-9 mAb. (cdc.gov)
- Oxidative stress, caspase-3 activation and cleavage of ROCK-1 play an essential role in MeHg-induced cell death in primary astroglial cells. (nih.gov)
- 19. AlphaII-spectrin is an in vitro target for caspase-2, and its cleavage is regulated by calmodulin binding. (nih.gov)
- This study aimed to induce apoptosis in breast cancer cells by purifying L- asparaginase from human breast milk Lactobacillus reuteri isolates via inhibition of Caspases 8 and 9. (bvsalud.org)
- In additional experiments, the team found that the NSAID inhibition of caspase was independent of COX enzymes. (nih.gov)
- The antiapoptotic effect of vitamin C was associated with reduced cytochrome C release from mitochondria and the inhibition of caspase-9 activity. (nih.gov)
- Breast cancer cell line was used to study the effect of the enzyme on the caspase 8 and caspase 9 gene expression . (bvsalud.org)
- The new treatment targets an enzyme called caspase-9, says Carol M. Troy, MD, PhD, professor of pathology & cell biology and of neurology in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Vagelos College of Physicians and Surgeons, who led the studies. (nih.gov)
- The team first ranked the drugs by their ability to inhibit the activity of the caspase-4 enzyme. (nih.gov)
- It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES . (nih.gov)
- Caspases (CASPs) are the main executors of the apoptotic process. (nih.gov)
- As effectors of the apoptotic machinery, caspases are considered potential therapeutic targets. (cshl.edu)
- Caspase 9 is activated during cell stress by mitochondria-derived proapoptotic factors and by CARD SIGNALING ADAPTOR PROTEINS such as APOPTOTIC PROTEASE-ACTIVATING FACTOR 1 . (nih.gov)
- Mitochondrial release of Cytochrome c and the resulting activation of caspase-9 and caspase-3 were determined by Western blots. (cdc.gov)
- In following the gene of biosensor is sub-cloned into a eukaryotic vector and transfected to HEK293T cell line and then its activity is measured upon apoptosis induction in the presence and absence of a caspase-9 inhibitor. (caltech.edu)
- Furthermore, the activation of the p38 kinase promoted the activation of p53 and its downstream target p21, and further caused caspase-9 and -3 activation, as demonstrated by evidence showing that the p38 inhibitor SB203580 not only blocked the phosphorylation of p38 but also reduced the activation of p53, p21 and caspase-9 and -3. (spandidos-publications.com)
- Importantly, a p38 inhibitor but neither an ERK inhibitor nor a JNK inhibitor, blocked the phosphorylation of p38 and also reduced the activation of p53, p21 and caspase-9 and -3. (spandidos-publications.com)
- Eye drops with a caspase-9 inhibitor prevent retinal injury from retinal vein occlusion. (nih.gov)
- Influence of caspases 8 and 9 gene promoter polymorphism on prostate cancer susceptibility and early development of hormone refractory prostate cancer. (cdc.gov)
- Polymorphisms of caspase 8 and caspase 9 gene and colorectal cancer susceptibility and prognosis. (cdc.gov)
- Caspase 8 and caspase 9 gene polymorphisms and susceptibility to gastric cancer. (cdc.gov)
- NB100-56186) that we used for localizing XIAP does not recognize XIAP, but instead most likely recognizes the cleaved Caspase 9 which conjugates with XIAP in the apoptosome. (elsevierpure.com)
- c , Colorimetric caspase-3 activity assay using pcWNV-Cp-DJY (Cp-DJY), pcWNV-CpWT (CpWT), or pcWNV-CpΔ3′ (CpΔ3') plasmid-transfected cells. (cdc.gov)
- Under normal conditions, caspase-9 is believed to be primarily involved in programmed cell death, a tightly regulated mechanism for naturally eliminating damaged or excess cells. (nih.gov)
- In human cells, the caspases were inhibited by the same NSAIDs in the same rank order as in the high-throughput screen. (nih.gov)
- 40. miR-106a-mediated malignant transformation of cells induced by anti-benzo[a]pyrene-trans-7,8-diol-9,10-epoxide. (nih.gov)
- Additionally, moringa can upregulate caspase 3 and 9, which are associated with programmed cell death in cancer cells. (naturalnews.com)
- Circulating EPO in the normal adult is mainly mass is made up of carbohydrate chains that produced by fibroblast-like interstitial cells of the renal cortex . (who.int)
- Carcinogenesis 2012 Sep 33 (9): 1699-706. (cdc.gov)
- Using an established in vivo model of Fas-mediated apoptosis, we demonstrate here that elimination of certain caspases was compensated in vivo by the activation of other caspases. (cshl.edu)
- Our findings provide direct experimental evidence for compensatory pathways of caspase activation. (cshl.edu)
- Organic solvent-induced proximal tubular cell toxicity via caspase-3 activation. (cdc.gov)
- Inhibiting ROCK-1 and caspases activation attenuated the MeHg-induced cell death. (nih.gov)
- 14. Activation and substrate specificity of caspase-14. (nih.gov)
- Collectively, these results suggest that p53-dependent and caspase-dependent induction of p38 MAPK directly participates in apoptosis induced by oridonin. (spandidos-publications.com)
- A long pro-domain caspase that contains a CASPASE RECRUITMENT DOMAIN in its pro-domain region. (nih.gov)
- Indeed, as early as the 1970s, investigators conducting research on the efficacy of RT in mouse tumor models observed reduced efficacy in immunodeficient nude mice compared to immunocompetent mice 9 pointing to a role for the adaptive immune response in the efficacy of RT. (nature.com)
- In studies of mice, the Troy lab discovered that when blood vessels are injured by retinal vein occlusion, caspase-9 becomes uncontrollably activated, triggering processes that can damage the retina. (nih.gov)
- La caspasa 9 es activada durante el estrés celular por factores proapoptóticos derivados de las mitocondrias y por PROTEÍNAS ADAPTADORAS DE SEÑALIZACIÓN CARD como el FACTOR APOPTÓTICO 1 ACTIVADOR DE PROTEASAS. (bvsalud.org)
- d , The cell lysates were assayed for caspase-9-like activity, and the pcDNA3.1-transfected cell lysate was used as the negative control. (cdc.gov)
- In this project, a luciferase-based biosensor for detecting and measuring caspase-9 activity is designed and constructed using the circular permutation strategy. (caltech.edu)
- Afterward, the biosensor is utilized for measuring the cellular caspase-9 activity upon apoptosis induction in a cancer cell line. (caltech.edu)
- The obtained results show that the designed biosensor detects the caspase-9 activity in the cell-free and cell-based systems. (caltech.edu)
- This newly discovered mechanism of NSAID activity suggests future studies into how these drugs affect caspases in the human body. (nih.gov)
- Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2009 Dec 27 (34): 5823-9. (cdc.gov)
- Median survival for patients with locally advanced disease is 9-12 months, and for patients with metastatic disease, the median survival is 3-6 months. (spandidos-publications.com)
- Polymorphisms in the CASPASE genes and survival in patients with early-stage non-small-cell lung cancer. (cdc.gov)
- Prognostic Impact of Polymorphisms in the CASPASE Genes on Survival of Patients with Colorectal Cancer. (cdc.gov)
- Nod-1 was found to bind to multiple caspases with long prodomains, but specifically activated caspase-9 and promoted caspase- 9-induced apoptosis. (elsevierpure.com)
- Anxiety, depression, and delirium all negatively influence recovery after stroke ( 9 , 10 ). (frontiersin.org)
- Further tests of 9 selected NSAIDs showed that all except aspirin inhibited multiple caspases. (nih.gov)
- Development of an inducible caspase-9 safety switch for pluripotent stem cell-based therapies. (nih.gov)
- International journal of colorectal disease 2011 Sep 26 (9): 1113-8. (cdc.gov)
- Caspase-9 and caspase3 were also induced by the silica treatment. (cdc.gov)